ONTARIO
QUIT
BASE HOSPITAL GROUP
ADVANCED ASSESSMENT
Shock
2007 Ontario Base Hospital Group
OBHG Education Subcommittee
ADVANCED ASSESSMENT
Shock
AUTHOR(S)
REVIEWERS
Mike Muir AEMCA, ACP, BHSc
Rob Theriault EMCA, RCT(Adv.), CCP(F)
Peel Region Base Hospital
Paramedic Program Manager
Grey-Bruce-Huron Paramedic Base Hospital
Grey Bruce Health Services, Owen Sound
Kevin McNab AEMCA, ACP
Donna L. Smith AEMCA, ACP
Hamilton Base Hospital
Quality Assurance Manager
Huron County EMS
References – Emergency Medicine
2007 Ontario Base Hospital Group
OBHG Education Subcommittee
Shock
Widespread Tissue Hypoperfusion
Results In
Inadequate oxygenation and supply of nutrients at a cellular level
Inadequate removal of metabolic waste products
Due To
Inadequate circulation of blood
Leads To
Generalized impairment of cellular function
Ultimate cell death
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ENERGY PRODUCTION
Human Body Likes Presence of Oxygen
To Produce Energy
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Aerobic Metabolism
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Energy production in the setting of
oxygen
High amount of energy production
 38 Adenosine Tri-phosphate
 Low waste (Acid Production)
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Anaerobic Metabolism
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Energy production without oxygen
Low amount of energy production
2 Adenosine Tri-phosphate (Glycolysis
Sugar Splitting)
High acid production
Pyruvic to Lactic Acid results in metabolic
acidosis
Cell functions cease due to lack of energy
and acidosis
Cell death
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S
H
O
C
K
Septic, Spinal
Hypovolemic
Obstructive, Mechanical
Cardiogenic
Anaphylactic
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Septic Shock
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Caused by serious systemic bacterial infection
(usually gram negative bacteria)
Causes a release of vasoactive agents that affect
microcirculation (arterioles and venules dilate
{increased container size}, capillary leak {loss of
volume}
Increased container size and loss of volume lead to
inadequate tissue perfusion
OBHG Education Subcommittee
Septic Shock
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Signs and Symptoms
 Fever (may not have fever), tachycardia, tachypnea,
confusion, petechiae around eyes, purpura
 Look for history of recent infection (bladder,
pneumonia)
Treatment
 Identify and correct infection (antibiotics)
 Manage hypovolemia and acid base imbalance (fluid
therapy, vasoactive and cardiac drugs)
OBHG Education Subcommittee
Neurogenic Shock/Spinal Shock
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Predominantly causes by Spinal Cord Injury, may
also be caused by head injury, CVA or drug overdose
Block of sympathetic outflow results in peripheral
vasodilatation
OBHG Education Subcommittee
Spinal Shock
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Vasomotor paralysis below level of spinal cord injury
Normal vasomotor tone through sympathetic control
is lost
Results in vasodilatation, increased container size
Even normal intravascular volume is insufficient to fill
vascular compartment
Unable to mount compensatory tachycardia
Heart rate remains unchanged with hypotension
Look for line where sympathetic response ends
Treatment
 Similar to Hypovolemia, caution not to cause fluid
overload
OBHG Education Subcommittee
Mechanical Shock/Obstructive
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Blood flow disrupted due to mechanical obstruction
Examples
 Tension Pnemothorax - Increased intrathoracic
pressure impedes low pressured venous return,
increased pressure can twist and compress heart
 Cardiac Tamponade - Compression of heart due to
accumulation of fluid or in pericardial sac (usually due
to trauma or infection)
OBHG Education Subcommittee
Mechanical Shock/Obstructive
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Examples cont’d
 Pulmonary Embolism - Blockage of blood flow in
pulmonary circulation (fat, air, thrombus)
 Aortic Dissection - Blood flow obstructed distal to left
ventricle (Dissection of Aortic Arch= b/p right arm
greater than left)
Treatment
 Correct cause of obstruction
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Cardiogenic Shock
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Cardiac action cannot deliver circulating blood
volume adequate for tissue perfusion
Examples
 Massive M.I
 Rhythm Disturbance (fast or slow)
 Cardiac Contusion
Treatment
 Improving pumping action of the heart and
managing cardiac rhythm irregularities
(medications, electrical therapy, fluid)
 Treat associated problems ex. CHF
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Cardiogenic Shock
- VISCIOUS CYCLE
•Heart Damage >50% Muscle Damage
→ Decreased Circulating Volume
→ Increased Compensatory Heart Rate
→ Damaged ISCHEMIC Heart Has Increased Workload,
Increased Oxygen Demand
→ FURTHUR Damage To Heart Muscle
→ B/p Doesn’t Change Or Drops
→ CON’T Cycle Till Complete Failure
→ >90% Mortality Rate
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Anaphylactic Shock
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Severe systemic allergic reaction due exposure to an
allergen
(ex. food,drugs,insect bites)
Causes exaggerated release of chemical mediators
(HISTAMINE, serotonin, kinins)
OBHG Education Subcommittee
Multi-System Involvement
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Respiratory
 Upper airway obstruction secondary to edema
 Severe bronchiole constriction
Integumentary
 Hives
 Local Swelling (capillary leak)
Gastrointestinal
 Nausea and vomiting, Abdominal pain, Diarrhea
OBHG Education Subcommittee
Multi-System Involvement
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Circulatory
 Hypotension (Capillary leak, vessel dilation)
Treatment
 remove exposure of allergen, epinephrine,
bronchodilators, antihistamines, fluid therapy
OBHG Education Subcommittee
Hypovolemic Shock (Loss of
Circulating Volume)
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Hemorrhagic
 Internal blood loss, eg. G.I bleed
 External blood loss, laceration
Non-Hemorrhagic
 G.I losses prolonged severe vomiting and diarrhea
 Renal losses excessive use of diuretics (^urine
prod.)
 Cutaneous losses heat exhaustion and burns
(3rd spaced shift)
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TREATMENT
Correct circulatory deficit and cause, surgery,
volume replacement
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Normal Circulating Volumes
Adult = 70 ml/kg
Pediatric = 80 ml/kg
Infant = 90 ml/kg
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Stages of Shock
1st Stage: 0-15 % of blood volume
2nd Stage: 15-30% of blood volume
3rd Stage: 30-40% of blood volume
4th Stage: >40%
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Early Signs & Symptoms of Shock
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Altered LOA, confusion, agitation
Normal possible slight increase in blood pressure
Tachycardia
Pale, moist skin
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Late Sign
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Hypotension
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3 STAGES OF SHOCK
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1 Compensated Shock
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Some decreased tissue perfusion, but bodies
compensatory mechanisms overcome
Cardiac output and systolic b/p maintained by
catecholamine release
Mild tachycardia, altered LOA, agitation, delayed cap
refill, cool skin, b/p normal or slightly elevated
Continued compensatory leads to acidosis as
perfusion decreases (chemoreceptors respond with
increased respiratory rate)
OBHG Education Subcommittee
2 Uncompensated Shock
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Unable to maintain systolic blood pressure
Systolic and diastolic blood pressure drops, pulse
pressure narrows till non existent (pulse pressure
systolic minus diastolic)
Compensatory mechanisms begin to fail, cerebral
blood flow decreases even with blood being shunted
to vital organs
Moderate tachycardia, confusion → unconsciousness
Delayed cap refill, cold extremities, cyanosis,
hypotension
OBHG Education Subcommittee
3 Irreversible Shock
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Progression of cellular ischemia and necrosis with
subsequent organ death, despite restoration of
oxygenation and perfusion
Membrane pump fails and various organelles
breakdown inside of cell
Bradycardia, dysrhythmia, coma, Frank Hypotension
Results in death even if volume corrected
OBHG Education Subcommittee
COMPENSATORY MECHANISMS
IN SHOCK
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Neurogenic Compensation (Central
Nervous System)
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Autonomic (Sympathetic, Fight or Flight)
Rapid onset
Increased heart rate (chronotropic), increased force
of contraction (inotropic), increased conduction
(dromotropic) Beta 1
Stimulates Adrenal Medulla to secrete
Norepinepherine and Epinephrine
Nor Epinephrine-Alpha 1 peripheral vasoconstriction,
Epinephrine- Beta 2 dilate vessels to coronary and
skeletal muscle, bronchodilation
OBHG Education Subcommittee
Baroreceptors and the Sympathetic
Nervous System
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Controls rapid moment to
moment B/P
 in blood pressure causes
baroreceptors (stretch) to
send fewer impulses to the
cardiovascular center in the
CNS
Response  Sympathetic
output
Cardiac Output
Vasoconstriction
= in blood pressure
OBHG Education Subcommittee
Chemical Compensation (Respiratory
System)
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Decreased Po2 sensed by peripheral
chemoreceptors, increased acidosis sensed by
central chemoreceptors
Stimulates increased respiratory rate, maximizes
FiO2, compensates for acid base imbalance
OBHG Education Subcommittee
Hormonal Compensation
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Epinephrine and Nor Epinephrine as above
Renin-Angiotensin System
Anti-diuretic Hormone
ACTH – Adrenocorticotropic Hormone
OBHG Education Subcommittee
Renin-Angiotensin System
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Decreased blood flow to Kidneys-> Hypoprofusion
sensed by Juxtaglomerular Cells, causes kidneys secrete
renin->Renin acts on Angiotensinogen (protein from
liver)->Angiotensine 1->at lungs converted to
Angiotensine 2 by ACE-> Angiotensine 2 powerful
vasoconstrictor and stimulates Adrenal Cortex to secrete
Aldosterone
Aldosterone stimulates kidneys to retain sodium with that
water overall increasing fluid volume
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Renin/Angiotensin System
Liver
Angiotesinogen
Kidney
Renin
Angiotesin I
Angiotesin
Converting
Enzyme
Peripheral
Vasoconstriction
Angiotesin II
Adrenal
Aldosterone
Na+ and H2O Absorption
OBHG Education Subcommittee
Anti-diuretic Hormone - ADH
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Secreted by posterior pituitary if stimulated by
hypothalamus (Senses increased osmotic pressure)
volume =  Tonicity (sodium)
Causes tubules of kidney to be more permeable to
water therefore more volume retained
OBHG Education Subcommittee
ACTH - Adrenocorticotropic Hormone
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Hypothalamus stimulates anterior pituitary to secrete
ACTH
ACTH stimulates metabolism of carbohydrates,
proteins and fats
Decreases permeability of capillary walls helping
prevent loss of intravascular fluid
OBHG Education Subcommittee
SPECIAL ASSESMENT CASES
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Relative Hypotension
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Hypotension is usually defined as blood pressure
less than 90 or 100 mmhg (average person)
Patients who have Hypertension will have
decompensatory drop in blood pressure, their drop of
30 or 40 mmHg may only put them in the 110,100
systolic range they are just as hypotensive though as
the person normal tensive with blood pressure of
80mmHg
This is called relative hypotension
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Beware of Beta Blocked Patient
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Will not have compensatory increase in heart rate
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Beware of the Pediatric Patient
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Compensate until point of failure
Shock may be present despite normal blood pressure
Look For:
Altered LOA, diminished peripheral pulses, delayed cap
refill, Tachycardia, check temperature of extremities
Late signs: Bradycardia, hypotension
OBHG Education Subcommittee
Shock in Pregnant Female
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30-40% blood volume increase
Only 15-20% increase in hematocrit (functionally
anemic)
Present in shock like picture without deficit
{Functional Hyperventilation, PaCO2 30mmhg, Lower
b/p, Increased heart rate 10-30bpm
Will appear in class 2 or 3 shock without injury
OBHG Education Subcommittee
Burn Patient
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Burn patient with 2nd and 3rd degree burns have
large amount of fluid loss due to third space shift
Damage causes fluid to shift from intracellular space
to interstitial space
Leads to hypotension and large amounts of swelling
in burned area
Parkland Formula
Ideal fluid replacement (4ml/kg X % of area burned)
1st half over 8 hours, 2nd half over next 16 hours
OBHG Education Subcommittee
Orthostatic Vitals
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Body unable to compensate for drop in blood
pressure while in sitting or standing position
Lying flat allows body to maintain somewhat normal
blood pressure
Sitting patient up will cause change in blood pressure
and heart rate
Drop of 20mmHg systolic or 10 mmHg diastolic is
significant
Increase of heart rate 20 per minute is significant
Patient must be in sitting position for 1-2 min
Do not do on patients exhibiting signs of
hypoperfusion (dizziness lying flat)
Done to rule out positional change in vitals
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ONTARIO
START
QUIT
BASE HOSPITAL GROUP
Well Done!
Ontario Base Hospital Group
Self-directed Education Program
OBHG Education Subcommittee